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1. Splenic monocytes drive pathogenic subretinal inflammation in age-related macular degeneration.

Author

Roubeix, Christophe, Nous, Caroline, Augustin, Sébastien, Ronning, Kaitryn, Mathis, Thibaud, Blond, Frédéric, Lagouge-Roussey, Pauline, Crespo-Garcia, Sergio, Sullivan, Patrick, Gautier, Emmanuel, Reichhart, Nadine, Sahel, José-Alain, Burns, Marie, Paques, Michel, Sørensen, Torben, Strauss, Olaf, Guillonneau, Xavier, Delarasse, Cécile, and Sennlaub, Florian

Subjects
Age-related macular degeneration, Angiotensin, Neuroinflammation, Splenic monocytes, Humans, Mice, Animals, Aged, Monocytes, Angiotensin II, Macular Degeneration, Inflammation, Choroidal Neovascularization
Abstract

Age-related macular degeneration (AMD) is invariably associated with the chronic accumulation of activated mononuclear phagocytes in the subretinal space. The mononuclear phagocytes are composed of microglial cells but also of monocyte-derived cells, which promote photoreceptor degeneration and choroidal neovascularization. Infiltrating blood monocytes can originate directly from bone marrow, but also from a splenic reservoir, where bone marrow monocytes develop into angiotensin II receptor (ATR1)+ splenic monocytes. The involvement of splenic monocytes in neurodegenerative diseases such as AMD is not well understood. Using acute inflammatory and well-phenotyped AMD models, we demonstrate that angiotensin II mobilizes ATR1+ splenic monocytes, which we show are defined by a transcriptional signature using single-cell RNA sequencing and differ functionally from bone marrow monocytes. Splenic monocytes participate in the chorio-retinal infiltration and their inhibition by ATR1 antagonist and splenectomy reduces the subretinal mononuclear phagocyte accumulation and pathological choroidal neovascularization formation. In aged AMD-risk ApoE2-expressing mice, a chronic AMD model, ATR1 antagonist and splenectomy also inhibit the chronic retinal inflammation and associated cone degeneration that characterizes these mice. Our observation of elevated levels of plasma angiotensin II in AMD patients, suggests that similar events take place in clinical disease and argue for the therapeutic potential of ATR1 antagonists to inhibit splenic monocytes for the treatment of blinding AMD.

Published
2024

2. DRD2 activation inhibits choroidal neovascularization in patients with Parkinson's disease and age-related macular degeneration

Author

Mathis, Thibaud, Baudin, Florian, Mariet, Anne-Sophie, Augustin, Sebastien, Bricout, Marion, Przegralek, Lauriane, Roubeix, Christophe, Benzenine, Eric, Blot, Guillaume, Nous, Caroline, Kodjikian, Laurent, Mauget-Faysse, Martine, Sahel, Jose-Alain, Plevin, Robin, Zeitz, Christina, Delarasse, Cecile, Guillonneau, Xavier, Creuzot-Garcher, Catherine, Quantin, Catherine, Hunot, Stephane, and Sennlaub, Florian

Subjects
Physiological aspects, Complications and side effects, Dosage and administration, Health aspects, Macular degeneration -- Dosage and administration -- Physiological aspects -- Complications and side effects, Parkinson disease -- Dosage and administration -- Physiological aspects -- Complications and side effects, Choroid -- Health aspects, Neovascularization -- Health aspects, Medical research, Dopamine receptors -- Health aspects, Medicine, Experimental, Parkinson's disease -- Dosage and administration -- Physiological aspects -- Complications and side effects
Abstract

Introduction Alongside Alzheimer's disease, Parkinson's disease (PD) and age-related macular degeneration (AMD) are the most common age-associated neurodegenerative diseases (1, 2). AMD is the leading cause of central vision loss [...], Neovascular age-related macular degeneration (nAMD) remains a major cause of visual impairment and puts considerable burden on patients and health care systems. L-DOPA-treated Parkinson's disease (PD) patients have been shown to be partially protected from nAMD, but the mechanism remains unknown. Using murine models that combine 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced (MPTP-induced) PD and laser-induced nAMD with standard PD treatment of L-DOPA/DOPA-decarboxylase inhibitor or specific dopamine receptor inhibitors, we here demonstrate that L-DOPA treatment-induced increase of dopamine-mediated dopamine receptor D2 (DRD2) signaling inhibits choroidal neovascularization independently of MPTP-associated nigrostriatal pathway lesion. Analyzing a retrospective cohort of more than 200,000 patients with nAMD receiving anti-VEGF treatment from the French nationwide insurance database, we show that DRD2 agonist-treated PD patients have a significantly delayed age of onset of nAMD and reduced need for anti-VEGF therapies, similar to the effects of the L-DOPA treatment. While providing a mechanistic explanation for an intriguing epidemiological observation, our findings suggest that systemic DRD2 agonists might constitute an adjuvant therapy to delay and reduce the need for anti-VEGF therapy in patients with nAMD.

Published
2024
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4. Correction: Autophagy protein 5 controls flow-dependent endothelial functions

Author

Nivoit, Pierre, Mathivet, Thomas, Wu, Junxi, Salemkour, Yann, Sankar, Devanarayanan Siva, Baudrie, Véronique, Bourreau, Jennifer, Guihot, Anne-Laure, Vessieres, Emilie, Lemitre, Mathilde, Bocca, Cinzia, Teillon, Jérémie, Le Gall, Morgane, Chipont, Anna, Robidel, Estelle, Dhaun, Neeraj, Camerer, Eric, Reynier, Pascal, Roux, Etienne, Couffinhal, Thierry, Hadoke, Patrick W. F., Silvestre, Jean-Sébastien, Guillonneau, Xavier, Bonnin, Philippe, Henrion, Daniel, Dengjel, Joern, Tharaux, Pierre-Louis, and Lenoir, Olivia

Published
2023
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5. Autophagy protein 5 controls flow-dependent endothelial functions

Author

Nivoit, Pierre, Mathivet, Thomas, Wu, Junxi, Salemkour, Yann, Sankar, Devanarayanan Siva, Baudrie, Véronique, Bourreau, Jennifer, Guihot, Anne-Laure, Vessieres, Emilie, Lemitre, Mathilde, Bocca, Cinzia, Teillon, Jérémie, Le Gall, Morgane, Chipont, Anna, Robidel, Estelle, Dhaun, Neeraj, Camerer, Eric, Reynier, Pascal, Roux, Etienne, Couffinhal, Thierry, Hadoke, Patrick W. F., Silvestre, Jean-Sébastien, Guillonneau, Xavier, Bonnin, Philippe, Henrion, Daniel, Dengjel, Joern, Tharaux, Pierre-Louis, and Lenoir, Olivia

Published
2023
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7. P2X7-deficiency improves plasticity and cognitive abilities in a mouse model of Tauopathy

Author

Carvalho, Kevin, Martin, Elodie, Ces, Aurélia, Sarrazin, Nadège, Lagouge-Roussey, Pauline, Nous, Caroline, Boucherit, Leyna, Youssef, Ihsen, Prigent, Annick, Faivre, Emilie, Eddarkaoui, Sabiha, Gauvrit, Thibaut, Vieau, Didier, Boluda, Susana, Huin, Vincent, Fontaine, Bertrand, Buée, Luc, Delatour, Benoît, Dutar, Patrick, Sennlaub, Florian, Guillonneau, Xavier, Blum, David, and Delarasse, Cécile

Published
2021
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8. The 10q26 Risk Haplotype of Age-Related Macular Degeneration Aggravates Subretinal Inflammation by Impairing Monocyte Elimination

Author

Beguier, Fanny, Housset, Michael, Roubeix, Christophe, Augustin, Sebastien, Zagar, Yvrick, Nous, Caroline, Mathis, Thibaud, Eandi, Chiara, Benchaboune, Mustapha, Drame-Maigné, Adèle, Carpentier, Wassila, Chardonnet, Solenne, Touhami, Sara, Blot, Guillaume, Conart, Jean Baptiste, Charles-Messance, Hugo, Potey, Anaïs, Girmens, Jean-François, Paques, Michel, Blond, Fréderic, Leveillard, Thierry, Koertvely, Elod, Roger, Jerome E., Sahel, José-Alain, Sapieha, Przemyslaw, Delarasse, Cécile, Guillonneau, Xavier, and Sennlaub, Florian

Published
2020
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12. Perilipin 2–positive mononuclear phagocytes accumulate in the diabetic retina and promote PPARγ-dependent vasodegeneration

Author

Blot, Guillaume, primary, Karadayi, Rémi, additional, Przegralek, Lauriane, additional, Sartoris, Thérèse-Marie, additional, Charles-Messance, Hugo, additional, Augustin, Sébastien, additional, Negrier, Pierre, additional, Blond, Frédéric, additional, Muñiz-Ruvalcaba, Frida Paulina, additional, Rivera-de la Parra, David, additional, Vignaud, Lucile, additional, Couturier, Aude, additional, Sahel, José-Alain, additional, Acar, Niyazi, additional, Jimenez-Corona, Aida, additional, Delarasse, Cécile, additional, Garfias, Yonathan, additional, Sennlaub, Florian, additional, and Guillonneau, Xavier, additional

Published
2023
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16. Complement Factor H Inhibits CD47-Mediated Resolution of Inflammation

Author

Calippe, Bertrand, Augustin, Sebastien, Beguier, Fanny, Charles-Messance, Hugo, Poupel, Lucie, Conart, Jean-Baptiste, Hu, Shulong J., Lavalette, Sophie, Fauvet, Alexandre, Rayes, Julie, Levy, Olivier, Raoul, William, Fitting, Catherine, Denèfle, Thomas, Pickering, Matthew C., Harris, Claire, Jorieux, Sylvie, Sullivan, Patrick M., Sahel, José-Alain, Karoyan, Philippe, Sapieha, Przemyslaw, Guillonneau, Xavier, Gautier, Emmanuel L., and Sennlaub, Florian

Published
2017
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20. Evidence of the involvement of dystrophin Dp71 in corneal angiogenesis

Author

Ortiz, Gabriella, Vacca, Ophélie, Bénard, Romain, Dupas, Bénédicte, Sennlaub, Florian, Guillonneau, Xavier, JA, Sahel, Tadayoni, Ramin, Rendon, Alvaro, Giocanti-Aurégan, Audrey, Brighton and Sussex University Hospitals - NHS Trust (BSUH), Institut des Neurosciences Paris-Saclay (NeuroPSI), Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Institut de la Vision, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Hôpital Lariboisière-Fernand-Widal [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Diderot - Paris 7 (UPD7), Université Sorbonne Paris Cité (USPC), Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts (CHNO), Fondation Ophtalmologique Adolphe de Rothschild [Paris], Hôpital Avicenne [AP-HP], and PERIGNON, Alain

Subjects
genetic structures, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, [SDV.NEU.PC] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior, MESH: Mice, Knockout, Cornea, Dystrophin, MESH: Dystrophin, Animals, Corneal Neovascularization, MESH: Animals, Aorta, Mice, Knockout, MESH: Corneal Injuries, MESH: Corneal Neovascularization, [SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior, MESH: Cornea, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, [SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, MESH: Aorta, eye diseases, Disease Models, Animal, sense organs, MESH: Disease Models, Animal, [SDV.NEU.SC] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, Research Article, Corneal Injuries
Abstract

International audience; Purpose: The aim of this study was to define the role of dystrophin Dp71 in corneal angiogenesis.Methods: Inflammation-induced corneal neovascularization experiments were performed in Dp71-null mice and C57BL/6J wild-type mice.Results: The corneal neovascular area covered by neovascularization was larger in the injured corneas of the Dp71-null mice compared to the corneas of the wild-type mice: 40.72% versus 26.33%, respectively (p

Published
2022

21. Autophagy protein 5 controls flow-dependent endothelial functions

Author

Nivoit, Pierre, primary, Mathivet, Thomas, additional, Wu, Junxi, additional, Salemkour, Yann, additional, Sankar, Devanarayanan Siva, additional, Baudrie, Véronique, additional, Bourreau, Jennifer, additional, Guihot, Anne-Laure, additional, Vessières, Emilie, additional, Lemitre, Mathilde, additional, Bocca, Cinzia, additional, Teillon, Jérémie, additional, Gall, Morgane Le, additional, Chipont, Anna, additional, Robidel, Estelle, additional, Dhaun, Neeraj, additional, Camerer, Eric, additional, Reynier, Pascal, additional, Roux, Etienne, additional, Couffinhal, Thierry, additional, Hadoke, Patrick, additional, Silvestre, Jean-sébastien, additional, Guillonneau, Xavier, additional, Bonnin, Philippe, additional, Henrion, Daniel, additional, Dengjel, Jörn, additional, Tharaux, Pierre-Louis, additional, and Lenoir, Olivia, additional

Published
2022
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23. The P2X7 Receptor, a Multifaceted Receptor in Alzheimer's Disease.

Author

Ronning, Kaitryn E., Déchelle-Marquet, Paul-Alexandre, Che, Yueshen, Guillonneau, Xavier, Sennlaub, Florian, and Delarasse, Cécile

Subjects
ALZHEIMER'S disease, PURINERGIC receptors, TAU proteins, NEUROFIBRILLARY tangles, AMYLOID plaque, CHEMOKINE receptors, EPISODIC memory, NEURODEGENERATION
Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by impaired episodic memory and two pathological lesions: amyloid plaques and neurofibrillary tangles. In AD, damaged neurons and the accumulation of amyloid β (Aβ) peptides cause a significant release of high amounts of extracellular ATP, which acts as a danger signal. The purinergic receptor P2X7 is the main sensor of high concentrations of ATP, and P2X7 has been shown to be upregulated in the brains of AD patients, contributing to the disease's pathological processes. Further, there are many polymorphisms of the P2X7 gene that impact the risk of developing AD. P2X7 can directly modulate Aβ plaques and Tau protein lesions as well as the inflammatory response by regulating NLRP3 inflammasome and the expression of several chemokines. The significant role of microglial P2X7 in AD has been well established, although other cell types may also be important in P2X7-mediated mechanisms. In this review, we will discuss the different P2X7-dependent pathways involved in the development of AD. [ABSTRACT FROM AUTHOR]

Published
2023
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26. Hypoxia Inhibits Subretinal Inflammation Resolution Thrombospondin-1 Dependently

Author

Touhami, Sara, Béguier, Fanny, Yang, Tianxiang, Augustin, Sébastien, Roubeix, Christophe, Blond, Frederic, Conart, Jean Baptiste, Sahel, José Alain, Bodaghi, Bahram, Delarasse, Cécile, Guillonneau, Xavier, Sennlaub, Florian, Conart, Jean, Sahel, José, Hôpital Lariboisière-Fernand-Widal [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de la Vision, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Equipe 14 - Inflammation dans la dégénérescence neuronale et le remodelage vasculaire (Inserm U968/CNRS UMR7210/UPMC UM80), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Service d'Ophtalmologie [CHU Pitié-Salpêtrière], CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), and Gestionnaire, HAL Sorbonne Université 5

Subjects
Male, QH301-705.5, Retinal Pigment Epithelium, choroidal neovascularization, Catalysis, Monocytes, Retina, Article, Inorganic Chemistry, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Physical and Theoretical Chemistry, Biology (General), Molecular Biology, age-related macular degeneration, QD1-999, Spectroscopy, Inflammation, hypoxia, Lasers, Organic Chemistry, General Medicine, macrophages, mononuclear phagocytes, thrombospondin 1, Computer Science Applications, Mice, Inbred C57BL, Chemistry
Abstract

Hypoxia is potentially one of the essential triggers in the pathogenesis of wet age-related macular degeneration (wetAMD), characterized by choroidal neovascularization (CNV) which is driven by the accumulation of subretinal mononuclear phagocytes (MP) that include monocyte-derived cells. Here we show that systemic hypoxia (10% O2) increased subretinal MP infiltration and inhibited inflammation resolution after laser-induced subretinal injury in vivo. Accordingly, hypoxic (2% O2) human monocytes (Mo) resisted elimination by RPE cells in co-culture. In Mos from hypoxic mice, Thrombospondin 1 mRNA (Thbs1) was most downregulated compared to normoxic animals and hypoxia repressed Thbs-1 expression in human monocytes in vitro. Hypoxic ambient air inhibited MP clearance during the resolution phase of laser-injury in wildtype animals, but had no effect on the exaggerated subretinal MP infiltration observed in normoxic Thbs1−/−-mice. Recombinant Thrombospondin 1 protein (TSP-1) completely reversed the pathogenic effect of hypoxia in Thbs1−/−-mice, and accelerated inflammation resolution and inhibited CNV in wildtype mice. Together, our results demonstrate that systemic hypoxia disturbs TSP-1-dependent subretinal immune suppression and promotes pathogenic subretinal inflammation and can be therapeutically countered by local recombinant TSP-1.

Published
2022
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31. CCR2+ monocytes infiltrate atrophic lesions in age‐related macular disease and mediate photoreceptor degeneration in experimental subretinal inflammation in Cx3cr1 deficient mice

Author

Sennlaub, Florian, Auvynet, Constance, Calippe, Bertrand, Lavalette, Sophie, Poupel, Lucie, Hu, Shulong J., Dominguez, Elisa, Camelo, Serge, Levy, Olivier, Guyon, Elodie, Saederup, Noah, Charo, Israel F., Rooijen, Nico Van, Nandrot, Emeline, Bourges, Jean‐Louis, Behar‐Cohen, Francine, Sahel, José‐Alain, Guillonneau, Xavier, Raoul, William, and Combadiere, Christophe

Published
2013
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32. PDGF Receptor Alpha Signaling Is Key for Muller Cell Homeostasis Functions

Author

Diaz-Lezama, Nundehui, Wolf, Anne, Koch, Susanne, Pfaller, Anna M., Biber, Josef, Guillonneau, Xavier, Langmann, Thomas, Grosche, Antje, Diaz-Lezama, Nundehui, Wolf, Anne, Koch, Susanne, Pfaller, Anna M., Biber, Josef, Guillonneau, Xavier, Langmann, Thomas, and Grosche, Antje

Abstract

Muller cells, the major retinal macroglia, are key to maintaining vascular integrity as well as retinal fluid and ion homeostasis. Although platelet derived growth factor (PDGF) receptor expression in Muller glia has been reported earlier, their actual role for Muller cell function and intimate interaction with cells of the retinal neurovascular unit remains unclear. To close this gap of knowledge, Muller cell-specific PDGF receptor alpha (PDGFR alpha) knockout (KO) mice were generated, characterized, and subjected to a model of choroidal neovascularization (CNV). PDGFR alpha-deficient Muller cells could not counterbalance hypoosmotic stress as efficiently as their wildtype counterparts. In wildtypes, the PDGFR alpha ligand PDGF-BB prevented Muller cell swelling induced by the administration of barium ions. This effect could be blocked by the PDGFR family inhibitor AC710. PDGF-BB could not restore the capability of an efficient volume regulation in PDGFR alpha KO Muller cells. Additionally, PDGFR alpha KO mice displayed reduced rod and cone-driven light responses. Altogether, these findings suggest that Muller glial PDGFR alpha is central for retinal functions under physiological conditions. In contrast, Muller cell-specific PDGFR alpha KO resulted in less vascular leakage and smaller lesion areas in the CNV model. Of note, the effect size was comparable to pharmacological blockade of PDGF signaling alone or in combination with anti-vascular endothelial growth factor (VEGF) therapy-a treatment regimen currently being tested in clinical trials. These data imply that targeting PDGF to treat retinal neovascular diseases may have short-term beneficial effects, but may elicit unwarranted side effects given the putative negative effects on Muller cell homeostatic functions potentially interfering with a long-term positive outcome.

Published
2021

35. The familial dementia gene revisited: a missense mutation revealed by whole-exome sequencing identifies ITM2B as a candidate gene underlying a novel autosomal dominant retinal dystrophy in a large family

Author

Audo, Isabelle, Bujakowska, Kinga, Orhan, Elise, El Shamieh, Said, Sennlaub, Florian, Guillonneau, Xavier, Antonio, Aline, Michiels, Christelle, Lancelot, Marie-Elise, Letexier, Melanie, Saraiva, Jean-Paul, Nguyen, Hoan, Luu, Tien D., Léveillard, Thierry, Poch, Olivier, Dollfus, Hélène, Paques, Michel, Goureau, Olivier, Mohand-Saïd, Saddek, Bhattacharya, Shomi S., Sahel, José-Alain, and Zeitz, Christina

Published
2014
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36. Mutations in TRPM1 are a common cause of complete congenital stationary night blindness

Author

Audo, Isabelle, Kohl, Susanne, Leroy, Bart P., Munier, Francis L., Guillonneau, Xavier;, Mohand-Said, Saddek, Bujakowska, Kinga, Nandrot, Emeline F., Lorenz, Birgit, Preising, Markus, Kellner, Ulrich, Renner, Agnes B., Bernd, Antje, Antonio, Aline, Moskova-Doumanova, Veselina, Lancelot, Marie-Elise, Poloschek, Charlotte M., Drumare, Isabelle, Defoort-Dhellemmes, Sabine, Wissinger, Bernd, Leveillard, Thierry, Hamel, Christian P., Schorderet, Daniel F., De Baere, Elfride, Berger, Wolfgang, Jacobson, Samuel G., Zrenner, Eberhart, Sahel, Jose-Alain, Bhattacharya, Shomi S., and Zeitz, Christina

Subjects
Gene mutations -- Analysis, Night blindness -- Genetic aspects, Biological sciences
Abstract

Several analyses are conducted to determine the various genes that are mutated in the patients suffering from autosomal-recessive complete congenital stationary night blindness. The results demonstrate that TRPM1 is the most commonly mutated gene.

Published
2009

37. Cover Image, Volume 69, Issue 7

Author

Couturier, Aude, primary, Blot, Guillaume, additional, Vignaud, Lucile, additional, Nanteau, Céline, additional, Slembrouck‐Brec, Amélie, additional, Fradot, Valérie, additional, Acar, Niyazi, additional, Sahel, José‐Alain, additional, Tadayoni, Ramin, additional, Thuret, Gilles, additional, Sennlaub, Florian, additional, Roger, Jerome E, additional, Goureau, Olivier, additional, Guillonneau, Xavier, additional, and Reichman, Sacha, additional

Published
2021
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38. CD36 deficiency leads to choroidal involution via COX2 down-regulation in rodents

Author

Houssier, Marianne, Raoul, William, Lavalette, Sophie, Keller, Nicole, Guillonneau, Xavier, Baragatti, Barbara, Jonet, Laurent, Jeanny, Jean-Claude, Behar-Cohen, Francine, Coceani, Flavio, Scherman, Daniel, Lachapelle, Pierre, Ong, Huy, Chemtob, Sylvian, and Sennlaub, Florian

Subjects
Biological sciences
Abstract

Background In the Western world, a major cause of blindness is age-related macular degeneration (AMD). Recent research in angiogenesis has furthered the understanding of choroidal neovascularization, which occurs in the 'wet' form of AMD. In contrast, very little is known about the mechanisms of the predominant, 'dry' form of AMD, which is characterized by retinal atrophy and choroidal involution. The aim of this study is to elucidate the possible implication of the scavenger receptor CD36 in retinal degeneration and choroidal involution, the cardinal features of the dry form of AMD. Methods and Findings We here show that deficiency of CD36, which participates in outer segment (OS) phagocytosis by the retinal pigment epithelium (RPE) in vitro, leads to significant progressive age-related photoreceptor degeneration evaluated histologically at different ages in two rodent models of CD36 invalidation in vivo (Spontaneous hypertensive rats (SHR) and [CD36.sup.-/-] mice). Furthermore, these animals developed significant age related choroidal involution reflected in a 100%-300% increase in the avascu1ar area of the choriocapillaries measured on vascular corrosion casts of aged animals. We also show that proangiogenic COX2 expression in RIDE is stimulated by CD36 activating antibody and that CD36-deficient RIDE cells from SHR rats fail to induce COX2 and subsequent vascular endothelial growth factor (VEGF) expression upon OS or antibody stimulation in vitro. [CD36.sup.-/-] mice express reduced levels of COX2 and VEGF in vivo, and [COX2.sup.-/-] mice develop progressive choroidal degeneration similar to what is seen in CD36 deficiency. Conclusions CD36 deficiency leads to choroidal involution via COX2 down-regulation in the RPE. These results show a novel molecular mechanism of choroidal degeneration, a key feature of dry AMD. These findings unveil a pathogenic process, to our knowledge previously undescribed, with important implications for the development of new therapies., Introduction Age-related macular degeneration (AMD) is the leading cause of vision loss among older adults in industrialized countries [1]. The most prominent pathologic features of AMD involve lesions of the [...]

Published
2008

39. Involvement of Pleiotrophin in CNTF-mediated differentiation of the late retinal progenitor cells

Author

Roger, JeRA[acute accent]Me, Brajeul, ValeRie, Thomasseau, Sylvie, Hienola, Anni, Sahel, Jose-Alain, Guillonneau, Xavier, and Goureau, Olivier

Subjects
Ciliary neurotrophic factor, Leukemia, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.07.003 Byline: JerA[acute accent]me Roger (a), Valerie Brajeul (a), Sylvie Thomasseau (a), Anni Hienola (b), Jose-Alain Sahel (a), Xavier Guillonneau (a), Olivier Goureau (a) Keywords: CNTF; Pleiotrophin; Retina; Differentiation; Photoreceptor; Bipolar cells Abstract: Ciliary neurotrophic factor (CNTF) participates in retinal development by inhibiting rod differentiation and promoting bipolar and Muller cell differentiation. In order to identify genes which are regulated by CNTF in the developing retina, we carried out a subtractive hybridization study. By this approach, we identified the Pleiotrophin (Ptn) as an upregulated gene in postnatal day 0 (P0) retinal explants upon addition of CNTF. Correlation of overall expression patterns between different retinal cell markers and Ptn in situ hybridization suggest that Ptn transcripts are initially expressed in progenitor cells then in postmitotic precursors of the INL expressing the Chx10 gene, and later in some differentiated retinal Muller glial (RMG) cells and rod-bipolar cells. Overexpression of Ptn by in vitro electroporation of P0 rat retinal explants partially blocks rod differentiation and promotes bipolar cell production, similar to effects of exogenous CNTF and leukemia inhibitory factor (LIF). Furthermore, in P0 retinal explants from mice lacking Ptn, the inhibitory effect of CNTF and LIF on rod differentiation is partially reduced and the cytokine-induced bipolar cell differentiation is largely prevented. Together, these results demonstrate that influence of CNTF family of cytokines on the differentiation of late retinal progenitor cell population is partially mediated by the release of Ptn. Author Affiliation: (a) Laboratoire de Physiopathologie Cellulaire et Moleculaire de la Retine, UMR S 592 INSERM, Universite Pierre et Marie Curie-Paris6, HA[acute accent]pital Saint-Antoine, Paris, France (b) Neuroscience Center, Department of Biosciences, University of Helsinki, Finland Article History: Received 21 March 2006; Revised 26 June 2006; Accepted 9 July 2006

Published
2006

40. Reproducing diabetic retinopathy features using newly developed human induced‐pluripotent stem cell‐derived retinal Müller glial cells

Author

Couturier, Aude, primary, Blot, Guillaume, additional, Vignaud, Lucile, additional, Nanteau, Céline, additional, Slembrouck‐Brec, Amélie, additional, Fradot, Valérie, additional, Acar, Niyazi, additional, Sahel, José‐Alain, additional, Tadayoni, Ramin, additional, Thuret, Gilles, additional, Sennlaub, Florian, additional, Roger, Jerome E, additional, Goureau, Olivier, additional, Guillonneau, Xavier, additional, and Reichman, Sacha, additional

Published
2021
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47. Stimulation of Insulin Signaling Reverses Inflammation-Induced Cone Death in Retinal Detachment

Author

CONART, Jean-Baptiste, primary, Blot, Guillaume, additional, Augustin, Sébastien, additional, Roubeix, Christophe, additional, Beguier, Fanny, additional, Charles-Messance, Hugo, additional, Touhami, Sara, additional, Sahel, José-Alain, additional, Berrod, Jean-Paul, additional, Guillonneau, Xavier, additional, Delarasse, Cécile, additional, and Sennlaub, Florian, additional

Published
2020
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48. Rescue of Defective Electroretinographic Responses in Dp71-Null Mice With AAV-Mediated Reexpression of Dp71

Author

Barboni, Mirella Telles Salgueiro, primary, Vaillend, Cyrille, additional, Joachimsthaler, Anneka, additional, Liber, André Maurício Passos, additional, Khabou, Hanen, additional, Roux, Michel J., additional, Vacca, Ophélie, additional, Vignaud, Lucile, additional, Dalkara, Deniz, additional, Guillonneau, Xavier, additional, Ventura, Dora Fix, additional, Rendon, Alvaro, additional, and Kremers, Jan, additional

Published
2020
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49. CD36 Deficiency Inhibits Retinal Inflammation and Retinal Degeneration in Cx3cr1 Knockout Mice

Author

Lavalette, Sophie, primary, Conart, Jean-Baptiste, additional, Touhami, Sara, additional, Roubeix, Christophe, additional, Houssier, Marianne, additional, Augustin, Sébastien, additional, Raoul, William, additional, Combadière, Christophe, additional, Febbraio, Maria, additional, Ong, Huy, additional, Chemtob, Sylvain, additional, Sahel, José-Alain, additional, Delarasse, Cécile, additional, Guillonneau, Xavier, additional, and Sennlaub, Florian, additional

Published
2020
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